Chap 18

Return to Essential Concepts

  • The eukaryotic cell cycle consists of several distinct phases. These include S phase, during which the nuclear DNA is replicated, and M phase where the nucleus divides (mitosis) and then the cytoplasm divides (cytokinesis).
  • In most cells, there is one gap phase (G1) after M phase and before S phase, and another (G2) after S phase and before M phase. These gaps give the cell more time to grow and prepare for the events of S phase and M phase.
  • The cell-cycle control system coordinates the events of the cell cycle by sequentially and cyclically switching on the appropriate parts of the cell-cycle machinery and then switching them off.
  • The control system depends on a set of protein kinases, each composed of a regulatory subunit called a cyclin and a catalytic subunit called a cyclin-dependent protein kinase (Cdk).
  • Cyclin concentrations rise and fall at specific times in the cell cycle, helping to trigger events of the cycle. The Cdks are cyclically activated by both cyclin binding and the phosphorylation of some amino acids and the dephosphorylation of others; when activated, Cdks phosphorylate key proteins in the cell.
  • Different cyclin-Cdk complexes trigger different steps of the cell cycle: M-Cdk drives the cell to mitosis; G1-Cdk drives it through G1; G1/S-Cdk and S-Cdk drive it into S phase.
  • The control system also uses protein complexes that trigger the proteolysis of specific cell-cycle regulators at particular stages of the cycle.
  • The cell-cycle control system can halt the cycle at specific checkpoints to ensure that intracellular and extracellular conditions are favorable and that the next step in the cycle does not begin before the previous one has finished. Some of these checkpoints rely on Cdk inhibitors that block the activity or more cyclin-Cdk complexes.
  • S-Cdk initiates DNA replication during S phase and helps ensure that the genome is copied only once. Checkpoints in G1 phase, S phase and G2 prevent cells from replicating damaged DNA.
  • M-Cdk drives the cell into mitosis with the assembly of of the microtubule-based mitotic spindle, which will move daughter chromosomes to opposite poles of the cell.
  • Microtubules grow out from the duplicated centrosomes, and some interact with microtubules growing from the opposite pole, thereby becoming the interpolar microtubules that form the spindle.
  • Centrosomes, microtubules-associated motor proteins, and the replicated chromosomes themselves work together to assemble the spindle.
  • When the nuclear envelope breaks down, the spindle microtubules invade the nuclear area and capture the replicated chromosomes. The microtubules bind to the protein complexes, called kinetochores, associated with the centromere of each sister chromatid.
  • Microtubules from opposite poles pull in opposite directions on each replicated chromosome, bringing the chromosomes to the equator of the mitotic spindle.
  • The sudden separation of sister chromatids allows the resulting daughter chromosomes to be pulled by the spindle. The two poles also move apart, further separating the two sets of chromosomes.
  • The movement of chromosomes by the spindle is driven both by microtubule motor proteins and by microtubule polymerization and depolymerization.
  • A nuclear envelope re-forms around the two sets of segregated chromosomes to form two new nuclei, thereby completing mitosis.
  • The Golgi apparatus breaks into many smaller fragments during M phase, ensuring an even distribution between the daughter cells.
  • In animal cells, cytoplasmic division is mediated by a contractile ring of actin filaments and myosin filaments, which assembles midway between the spindle poles and contracts to divide the cytoplasm in two; in plant cells, by contrast, cell division occurs by the formation of a new call wall inside the parent cell, which divides the cytoplasm in two.
  • Animal cell numbers are regulated by a combination of intracellular programs and extracellular signals that control cell survival, cell growth, and cell proliferation.
  • Many normal cells die by apoptosis during the lifetime of an animall they do so by activating an internal suicide program and killing themselves.
  • Apoptosis depends on a family of proteolytic enzymes called caspases, which are made as inactive precursors (procaspases). The procaspases are themselves often activated by proteolytic cleavage mediated by caspases.
  • Most animal cells require continuous signaling from other cells to avoid apoptosis; this may be a mechanism to ensure that cells survive when and where they are needed.
  • Animal cells proliferate only if stimulated by extracellular mitogens produced by other cells, ensuring that a cell divides only when another cell is needed; the mitogens activate intracellular signaling pathways to override the normal brakes that otherwise block cell-cycle progression.
  • For an organism or an organ to grow, cells must grow as well as divide. Animal cell growth depends on extracellular growth factors which stimulate protein synthesis and inhibit protein degradation.
  • Cell and tissue size can also be influenced by inhibitory extracellular signal proteins that oppose the positive regulators of cell survival, cell growth and cell division.
  • Cancer cells fail to obey these 'normal' social controls on cell behavior and therefore outgrow, out-divide and out-survive their normal neighbors.
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